Induction of heat shock protein 72kDa expression is associated with attenuation of ischaemia-reperfusion induced microvascular injury.

Leukocyte-endothelial interaction is a pivotal step in the pathogenesis of ischemia-reperfusion (I/R) injury. Exposure of cells to a subcritical heat stress may protect cells from subsequent I/R injury, through induction of a 72-kDa heat shock protein (HSP72). The aim of this study was to investigate the effect of thermotolerance on leukocyte adherence and migration during an I/R period in rat mesenteric postcapillary venules. Sprague-Dawley rats were randomized into control (sham I/R), I/R, and thermotolerance+I/R groups. Thermotolerance was induced 18 hr prior to I/R, which was in turn established by occlusion of the superior mesenteric vascular pedicle for 10 mins, followed by 60 mins of reperfusion. The blood flow, leukocyte rolling velocity, and the number of adherent and migrated leukocytes in postcapillary venules were measured by intravital microscopy. I/R significantly decreased the rolling velocity of leukocytes; increased the number of adherent leukocytes at 10, 30, and 60 mins after reperfusion; and also increased the number of migrated leukocytes at 60 mins after reperfusion. Thermotolerance induction expression of HSP72 in pulmonary, intestinal, and mesenteric tissues was determined by Western immunoblotting. Thermotolerance significantly prevented the I/R-induced decrease in rolling velocity of leukocytes, the increase in the number of adherent leukocytes at 30 and 60 mins, and the increase in the number of migrated leukocytes at 60 mins. This results suggest that thermotolerance attenuates I/R injury by modulating leukocyte-endothelial interaction in vivo, possibly by increasing tissue expression of HSP72.